BACKGROUND: Sevoflurane is one of the commonly used volatile anesthetics in cancer patients. The protective effect of sevoflurane preconditioning has raised concerns about whether sevoflurane could act advantageously for survival even of cancer cells. Therefore, we investigated the effects of sevoflurane on proliferation in colon cancer cell lines. METHODS: HCT116 and HT29 cells were plated in 96-well plates at a density of 1 x 10(4) cells/well and incubated overnight. On the next day, cells were exposed to 1% or 2% sevoflurane for 6 hr. After 24 hr recovery, we performed MTT assay. The absorbance of the formazan product was measured at a wavelength of 570 nm using 650 nm as the reference. In addition, to investigate the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, we conducted the same experiment under co-administration of K(ATP) inhibitor, glibenclamide. RESULTS: Only 1% sevoflurane significantly enhanced cell proliferation compared to the control in HCT116 and HT29 cells. Enhanced proliferation by sevoflurane was completely blocked by co-administration with glibenclamide in HCT116 cells. CONCLUSIONS: We had shown that 1% sevoflurane for 6 hr potentially enhances cell proliferation via K(ATP) channels in cancer cells.
BACKGROUND:Sevoflurane is one of the commonly used volatile anesthetics in cancerpatients. The protective effect of sevoflurane preconditioning has raised concerns about whether sevoflurane could act advantageously for survival even of cancer cells. Therefore, we investigated the effects of sevoflurane on proliferation in colon cancer cell lines. METHODS: HCT116 and HT29 cells were plated in 96-well plates at a density of 1 x 10(4) cells/well and incubated overnight. On the next day, cells were exposed to 1% or 2% sevoflurane for 6 hr. After 24 hr recovery, we performed MTT assay. The absorbance of the formazan product was measured at a wavelength of 570 nm using 650 nm as the reference. In addition, to investigate the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, we conducted the same experiment under co-administration of K(ATP) inhibitor, glibenclamide. RESULTS: Only 1% sevoflurane significantly enhanced cell proliferation compared to the control in HCT116 and HT29 cells. Enhanced proliferation by sevoflurane was completely blocked by co-administration with glibenclamide in HCT116 cells. CONCLUSIONS: We had shown that 1% sevoflurane for 6 hr potentially enhances cell proliferation via K(ATP) channels in cancer cells.